General Considerations

• Increase in the fluid in the lung
• Generally, divided into cardiogenic and non-cardiogenic categories.
• Congestive heart failure is the leading diagnosis in hospitalized patients older than 65
  

Pathophysiology

• Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg)
• Further accumulation occurs in the interstitial tissues of the lungs
• Finally, with increasing fluid, the alveoli fill with edema fluid (typically wedge pressure is 25 mm Hg or more)
  

Causes

• Cardiogenic pulmonary edema.

• Heart failure
• Coronary artery disease with left ventricular failure.
• Cardiac arrhythmias
• Fluid overload -- for example, kidney failure.
• Cardiomyopathy
• Obstructing valvular lesions -- for example, mitral stenosis
• Myocarditis and infectious endocarditis

• Non-cardiogenic pulmonary edema -- due to changes in capillary permeability

• Smoke inhalation.
• Head trauma
• Overwhelming sepsis.
• Hypovolemia shock
• Re-expansion
• By drainage of a large pleural effusion with thoracentesis
• Of the lung collapsed by a large pneumothorax
• High altitude pulmonary edema
• Disseminated intravascular coagulopathy (DIC)
• Near-drowning
• Overwhelming aspiration
• Heroin overdose
• Adult (acute) respiratory distress (deficiency) syndrome (ARDS)
• Clinical syndrome consisting of
• Pulmonary edema associated with severe respiratory distress
• Cyanosis refractory to oxygen administration
• Decreased lung compliance
• Lower pulmonary capillary wedge pressure (PCW < 18mm Hg) than cardiogenic pulmonary edema
• Most patients who survive have normal-appearing lungs
• Some patients develop pulmonary fibrosis
  

Clinical Findings

• Shortness of breath
• Hemoptysis
• Orthopnea
• Dyspnea on exertion
• Cough, wheezing
• Anxiety and restlessness
• Cyanosis

Imaging Findings

• Radiographic findings can lag behind physiologic changes
• The key findings of cardiogenic pulmonary edema
  • Kerley B lines (septal lines)
• Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface
• Pleural effusions
• Usually bilateral, frequently the right side being larger than the left
• If unilateral, more often on the right
• Fluid in the fissures
• Thickening of the major or minor fissure
• Peribronchial cuffing
• Visualization of small doughnut-shaped rings representing fluid in thickened bronchial walls
• Collectively, the above four findings comprise pulmonary interstitial edema
• The heart may or may not be enlarged
• When the fluid  enters the alveoli themselves, the airspace disease is typically diffuse, and there are no air bronchograms

• Non-cardiogenic pulmonary edema

• Bilateral, peripheral air space disease with air bronchograms or central bat-wing pattern
• Kerley B lines and pleural effusions are uncommon
• Typically occurs 48 hours or more after the initial insult
• Stabilizes at around five days and may take weeks to completely clear
• On CT
• Gravity-dependent consolidation or ground glass opacification
• Air bronchograms are common

Differential Diagnosis

• Diffuse pneumonia
• Massive aspiration
• Pulmonary hemorrhage

Treatment

• Cardiogenic pulmonary edema and non-cardiogenic pulmonary edema, with the exception of ARDS, can resolve within hours to several days
• Cardiogenic pulmonary edema is usually treated with a combination of
  • Oxygen
• Diuretics
• Lasix, etc.
• Nitrates
• Nitroglycerin, etc.
• Natriuretic peptides
• Nesiritide, etc.
• Morphine
• Inotropic agents
• Dopamine, dobutamine, digoxin, etc.
• Angiotensin converting enzyme (ACE) inhibitors
• Beta-blockers
• Carvedilol, etc.

• For non-cardiogenic pulmonary edema, the predisposing condition should be treated
  • Treatment is supportive
  • Ventilator management.
  • Antibiotic therapy, when necessary
  • Corticosteroids